Transcribed by Albert Cheng 5/12/14

Craniofacial Lecture 40 – Dental Pulp II by Dr. Lin

He was very hard to understand so there may be some parts that are hard to understand or I had to put together to make sense

Slide 56: Circulation of the Pulp[Dr. Lin] Good morning, this morning we are going to continue about dental pulp biology basically the blood supply and nerve innervation of the dental pulp. So it’s going to be a short lecture. Let’s talk about the blood supply to dental pulp. In the dental pulp, there are so called arterioles that are smaller than arteries and we have the venules and lymphatics

Slide 57: Takahasi 1982 pictureWhat happens is…take a look here. All the arterioles enter the root canal through the apical foramen. There are tons of apical foramen not just one. And you start to wonder, there are so many apical foramen so when I do a root canal, which one am I going to worry about? But I think you will eventually get to that. So all the arterioles enter the apical foramina through the apex. You see the slide? There are a lot of root here. Those arterioles not only enter the canal through one foramen. The veins carry the metabolic byproducts, waste byproducts, out the canal through the apical foramen. And the nerves enter through the apical foramen too.

Slide 58: Picture with a 100 in LR cornerThis is the apex. You see how many apical foramens here? There are tons of them here. Basically you have one major apical foramen, then you have so many accessory apical foramen. What happens is that the small apical foramina, the arterioles enter the canal through the small apical foramina. The large apical foramina are occupied by the venules. The arterioles enter the canal through the small apical foramina but the venules since they’re carrying all the waste products from the pulp get out of the canal through the large apical foramina.

Slide 59: Blood circulationWhen we take a look at the modern tooth, the pattern of the distribution of the blood supply is interesting. For example, this is the mesial root and this is the distal root. Once the arterioles enter the canal, they form a separate main trunk and they go to the pulp chamber. Another group comes from the other side. At this point, one group of arterioles goes all the way to the pulpal horn. The other group will cross the floor of the pulp chamber to join the group from the other side.

Slide 60: Picture with pulp horn and chamberSo let me show you here. You see this is the group of arterioles. Once they reach the pulpal floor, they start to divide into group 1 that goes all the way to the pulpal horn. The other group crosses the pulp chamber to join the other group from the other side. Why do we have so many blood vessels here and not in the root? Because the

root is embedded inside the bone and there’s very little locations for them to suffer any external stimulus. But in the crown area, it’s exposed to oral environment. So that part of the tooth, the crown, is constantly exposed to the outside. We need more blood supply in the pulp chamber. Our body’s defense mechanisms are all carried in the blood supply. If there’s no blood circulation to a tissue, the tissue is going to be dead because there’s no defense mechanism. Blood vessels carry what? You got the immunoglobuilins and blood borne cells and those are all our body’s defense components. It’s important to have a good blood supply in the crown area so this way our body can deliver the defense mechanism to the crown area to overcome any external stimuli

Slide 61: Sub-odontoblastic capillary networkOnce those blood vessels reach the odontoblasts there, they form the so called capillary network. And this network is formed just beneath the odontoblasts. Why do they form this capillary network underneath the odontoblasts? Because the odontoblasts are around dentin and periphery of the pulp. Once irritants get through the crown, they reach the pulp and what cells? The odontoblast because they are located at the periphery of the pulp and they form this capillary network just beneath the odontoblasts

Slide 62: Pulpal Blood FlowThere are some factors that can increase the pulpal blood flow. It’s very easy to understand. In order to increase the pulp blood flow, the pulp recruit the defense mechanism to get to the coronal area. Foreign factors can cause an increase in blood flow. Activation of sensory nerve fibers…I think that this we’ll get to in physiology during D3. Sensory fibers can release neuropeptides such as CGRP and SP (calcitonin related peptide). You will learn more about the neuropeptides in immunology. The neuropeptides have many functions. Bacterial products such as LPS (lipopolysaccharide) is one of the component of Gram-negative bacteria. This LPS can cause an increase in pulpal blood flow because it can cause vasodilation and increase vascular permeability. Same thing with CGRP/SP, they all can cause vasodilation and increase vascular permeability. Remember, when you have inflammation inside the pulp, there are a lot of inflammatory mediators released in the inflamed areas. There are so many prostaglandins, bradykinin, leukotrienes and histamines. All these bioactive materials can cause the vasodilation and increase vascular permeability. Let’s say you’re doing a cavity preparation and you don’t use water coolant, you can cook/kill the pulp inside the tooth. The heat can irritate the sensory nerve fibers and they will release all those mediators, which can cause vasodilation and increase vascular permeability. I mentioned last lecture…because the pulp is enclosed in the dentin wall, the interstitial pressure of the pulp is 5.6mmHg but once the inflammation due to vasodilation increase vascular permeability; all the blood and plasma proteins will leave the circulation and enter the interstitial tissue. Unfortunately, the pulp is enclosed in the dentin wall so there is no place for the pressure to disperse ok?

Slide 63: Pulpal Blood Flow (decrease)

But there’s some situation that can decrease the pulpal blood. If you stimulate this sympathetic nerve fiber, it will cause vasoconstriction. Local anesthesia also cause a decrease in pulpal blood flow. When there is necrosis in the pulp, the blood vessels also resorb and we’ll see a decrease in blood flow. Orthodontic treatment is also known as minor tooth movement. So you want to move those teeth slowly because you can kill it by moving too fast. That is the blood supply of the pulp

Slide 64: Nerve supply of the pulpNow we talk about the nerve supply of the pulp. The primary nerve supply to the pulp is very similar to the blood supply of the pulp.

Slide 65: Nerve supply of the pulpThe reason is the nerve fibers run side by side with the blood vessels into the root canal. This nerve fiber comes from the trigeminal ganglion and enters the tooth side by side with the arterioles. Remember I mentioned arterioles enter through the small apical foramina. Once they enter the apical foramina, they form a common nerve trunk.

Slide 66: Nerve supply of the pulpThey continue to proceed coronally and form a plexus of Raschkow at the subodontoblastic layer. I have a picture to show you later, don’t worry. From the plexus, numerous unmyelinated nerve fibers are sent to the odontoblast layer and very few to the predentin and inner dentin. Most of the nerve fibers into the pulp are so called myelinated nerve fibers.

Slide 67: Picture of tooth and caption “Nerve supply of the pulp”They enter the apical foramina accompanying the small arterioles. Once they enter the canal, they send very few branches in the canal. But once they reach there, they follow the pattern of the arterial supply. The reason is very simple. Because the crown is exposed to oral environment and it constantly receive external stimuli, we have to have something to tell us…let’s say you drink something hot and cold…how the pulp sense the hot and cold? Because this area is heavily innervated with numerous blood vessels and arterioles. The reason is in order to protect the pulp from further injury or damage.

Slide 68:So here, those are the nerve fibers that enter the canal and this you got a myelin sheath. And this is non-myelinated nerve fibers. More than 70% of those nerve fibers entering the root canal are so call myelinated nerve fibers. Remember the difference between myelinated and unmyelinated nerve fibers. Myelinated fibers conduct the impulse faster because the impulse jumps the node or Ranvier.

Slide 69: Plexus of RaschkowThis is the odontoblast and they form the Plexus of Raschkow in this area. The reason is because any external ??(can’t understand the next word) into the tooth,

the pulp is going to detect it right away because you got a plexus of nerve fibers in this area.

Slide 70: Types of peripheral nerve fibersSo basically there are several types of nerve fibers inside the pulp. You have the so called large myelinated A β, small myelinated A β , and small unmyelinated C fibers . This AB and C fibers are more related to the pulp

Slide 71: A-Beta fibersThis A-beta fibers is myelinated and has fast conducting velocity. They have lower threshold action potential that means tiny/light touches will activate this fiber. For example, innocuous touch. We do not know much about this fibers.

Slide 72: A-Delta Nerve fibersThis fiber we know more about. Remember in the pulp are the A-delta and C fibers. This A-delta are the myelinated nerve fibers because they have the myelin sheath produced by the Schwann cells. And basically they’re concentrated around the odontoblast layers. This is important because I will talk about the hydrodynamic concept. Remember I said last lecture I will explain to you the hydrodynamic concept. It’s easy to understand. These fibers contain CGRP and NGF. This NGF also has the receptor and is produced by the fibroblast. The diameter of this one is about 1-5 micron. It’s big ok. And the conducting velocity is around 12-30 meter/seconds. Remember this 12-30 m/sec***.

Slide 73: A-Delta Nerve fibersThis A-delta fiber is very sensitive to mechanical stimulation. I will talk about this and show you the picture about this so called hydrodynamic stimulation. Also has a low-threshold for activation, if you light touch it, the pulp is going to feel it. Once the A-delta fibers are stimulated, what happens? The patient experiences sharp stabbing pain. And this, remember this, is associated with dentin sensitivity***. Dentin sensitivity has nothing to do with pulpal inflammation. You apply something cold on the tooth, the patient will immediately feel it as sharp stabbing pain. What happens in (can’t understand his next few words)?? Ok, so in that kind of situation, it’s not related to pulpal inflammation, it’s called cold dentin sensitivity. And this can happen to some patients with perio problems and the root is exposed. In that kind of situation, when the patient takes something cold, they will tell you “god, everytime I take something cold, it hurts me so fast”. Then you have to ask the patients, “how long does it last?” And that is very important. If it only last only a few seconds, then it is dentin sensitivity. In this kind of situation, what does a periodontist do? You ask the patient to use Sensodyne because the dentinal tubules are exposed so you use the Sensodyne to try to block the dentinal tubules. Please be sure to remember dentin sensitivity. Anytime a patient complains of pain to hot and cold, be sure to ask how long does it last? And that is very important. If it last only a few seconds, then it’s dentin sensitivity. It has nothing to do with inflammation of the pulp. If it

lasts several minutes to hours, then it can be a different story. It can mean inflammation of the pulp and we’re getting there

Slide 74: C Nerve fibersThis is C-fiber, very important one. Be sure to remember this one. This is unmyelinated fiber. The C-fiber is located around the center of the pulp. Remember where the A-delta fibers are located? Close to the odontoblast layer. They also contain CGRP and substance p and also express those NGF receptors. The diameter here is 0.3-1micron. Remember the A-delta were 1-5 microns so they were bigger. The C fibers are smaller. The conducting velocity is 0.5 to 2.5m/sec so it is much slower than the A-delta fibers.

Slide 75: C Nerve FibersAnd they are also very sensitive to those inflammatory mediator such as histamine/bradykinin/leukotriene/prostaglandin but not to the hydrodynamic stimulation. It also has a high threshold for activation. You have to have high multitude of stimulation in order to activate this C-fiber. Remember this one…when the C-fibers are activated, they produce dull lingering pain. Remember when the A-delta fibers are activated, what happens? The patient experiences sharp stabbing pain**. When the C-fibers are activated, the patient will experience dull lingering pain and this is important when you diagnose whether the pulp is inflamed. If you use hot/cold to stimulate the tooth, and the patient tells you the pain is persistent for minutes to hours, then you know the pulp is involved. When the C-fibers are activated, it usually indicate there is pulpal inflammation. It’s important to differentiate dentin sensitivity and pulpal inflammation. The nature and the period of the pain will tell you whether the pulp is inflamed when you’re in clinic.

Slide 76: Hydrodynamic TheoryRemember last time, I said that 1 dentinal tubules is occupied by 1 odontoblast process. And I also just mentioned about the A-delta fibers. Those A-delta fibers are around the odontoblast. So what happens when you do a Class I cavity preparation? You remove the enamel and the dentin is exposed. There is dentinal fluid inside the tubules. If you blow air on this exposed surface, it can cause pain. The reason is this. When you blow the air to the exposed dentin, what happens? The fluid inside the dentinal tubules moves to the pulpal side. The movement of the tissue fluid inside the dentinal tubules can be seven meters/sec. The length of the dentinal tubules is no more than 5mm, so the movement is very fast. So the movement of the fluid towards the pulpal side will mechanically stimulate the A-delta fibers, which has low threshold for activation. So this will immediately activate the A-delta fibers. Cold will push the dentinal fluid out and hot will push the fluid inward towards the pulp. Just the tiny movement of the fluid will activate the A-delta fibers (sharp stabbing pain that last a few seconds dentin sensitivity). In that kind of situation, it’s not related to pulpal inflammation. How about if you blow cold air here to stimulate this fluid but unfortunately there is inflammation inside the pulp, what will happen? You

can also stimulate C-fibers and the patient will experience dull lingering pain that continue to persist for several minutes to hours. The time and nature of the pain is important. When this A-delta fibers are stimulated, the patient will tell you “gosh it’s sharp stabbing pain”. When the pulp is inflamed and you have lingering pain, the reason is simple. Those inflammatory mediators/cytokine can sensitize the nerve fibers.

Slide 77: Inflammatory Pain MechanismsSo here this is not only in the pulp but in the outer part of the body. If you have inflammation of the finger or the foot, the area is more sensitive to stimulation because in the inflamed tissue, you have all those inflammatory mediators/cytokine and those can sensitize your sensory nerve fibers (sensitize just means making more nerve fiber easier to stimulate). Not only is the tissue that’s inflamed is sensitive but the areas around it. Our nervous system plays an important role in our body defense mechanism. The nervous system and immune system are closely related.

Slide 78: Inflammatory Pain mechanismSo here when this area is inflamed, all those inflammatory cells dump all those inflammatory mediators/cytokine into this area. Then, this sensory nerve fibers become sensitize to any kind of stimulation.

Slide 79: Hyperalgesia/AllodyniaBe sure to know these 2 terms when you’re talking about pain. Hyperalgesia that means increase in the perceived magnitude of pain or painful stimulus. Let’s compare an inflamed and a healthy tooth. If you use the same method or irritation to stimulate those 2 teeth. The inflamed pulp/tooth will be more sensitive/painful than a regular tooth because the pulp test of irreversible pulpitis will increase the magnitude of painful stimuli. Allodynia is the reduction in pain threshold so that the previously non-noxious stimuli are perceived as painful.

Slide 80: So hyperalgesia and allodynia can be caused by both peripheral and central sensitization.

Slide 81: Peripheral SensitizationSo let’s say you have an inflamed finger/pulp, those inflammatory mediators produced at the injury site can sensitize the sensory nerve fibers. Therefore, the area will be more painful to stimuli.

Slide 82: Peripheral Sensitization (Arm picture)The picture here is easy to understand. If you have two arm, one arm has sunburnt area. If you touch the non-sunburnt side, you won’t feel the pain. The area with sunburn, the same magnitude of stimuli will cause pain because the area is inflamed. That is so called allodynia, the stimulation is non-noxious but because the

inflammation is there, when you touch it you will feel pain. In the same area, you can also have so called hyperalgesia. If you slap the healthy arm, you may feel some pain. But if you slap the sunburnt area, you will feel more pain because of all of those inflammatory mediator/cytokine released in that area. When you get endodontics, the tooth that has pulpal inflammation can have allodynia and at the same time hyperalgesia.

Slide 83: Diagram with arrows and yellow boxesWhen you have pain inside the tooth, and that pain continues to send impulses to the CNS. The CNS will become sensitize. Later on, if there’s any stimulation, the CNS will (not sure what he said but he said you will have hyperalgesia and allodynia and NOT TO WORRY about this because we will learn more about this next year).

Slide 84: Central sensitizationFor example, you have a toothache and not only do you have hyperalgesia and allodynia occurring in this tooth. Same thing in the CNS, you can have the same thing.

Slide 85: How does inflammatory pain present in the dental pulp?In the clinic, how do you know the pain is associated with inflammation. Let’s say a patient is in the clinic and you want to diagnose if the patient has pulpal inflammation.

Slide 86: Symptoms of Inflamed PulpThe patient will tell you they have spontaneous pains without hot/cold or “I have the constant pain there”. When you get to D2, you will learn how to diagnose pulpal disease. Don’t worry about that. Usually, the tooth will be sensitive to hot and cold when the patient drink. Remember I talk about A-delta and C fibers. Anytime a patient comes to clinic…”god everytime I drink something hot/cold, this tooth hurts me”…the next question you ask, “What is the nature of the pain?” If it’s a sharp stabbing pain, then it’s more related to the A-delta fiber. If it’s dull lingering continuous pain, then it’s related to activation of C-fibers and pulpal inflammation. You will get to irreversible pulpitis in D3. The clinical finding, you can use heat/cold to test the tooth and you will cause more pain. So in clinic, it is very important when the patient tells you they have pain from hot/cold, you have to be able to reproduce the same pain in order to reach the diagnosis.

Slide 87 (extra slide) Response of pulp sensory nerve fibers to external stimuliOne more important thing if you poke your hand, you’ll feel pain. If you use ice to touch your hand, you’ll feel cold. If you use heat to stimulate your hand, you know it’s hot. But in the pulp, there’s only one thing. The only thing the patient can tell you from the thermal/mechanical stimuli is PAIN. The pulp cannot tell you cold or hot because there are nociceptive nerve fiber – pain nerve fibers. There’s no hot/cold receptors in there.

Slide 88 (extra slide): Interactions between sensory nerve system, and innate and adaptive immune systemThere’s an interaction between the nervous system and innate/adaptive system. What happens is when the sensory nerve fibers in the pulp are stimulated, they will release substance P/CGRP and all those neuropeptide that can cause vasodilation and increase vascular permeability and also cause chemotaxis. The nervous system deals with wound healing, not only perceive the pain stimulus. And also the substance P and CGRP can induce the endothelial to express ICAMs, the adhesion molecule during inflammation. SO this way the inflammatory cells/PMNs can get out of circulation. Substance P can cause mast cells to release histamine and PGE2. So this is related to the innate immune response. SP and CGRP can cause macrophage to release pro-inflammatory cytokine (IL-1/6, TNF). Most B and T cells have the receptors for SP and CGRP. SP causes T cell proliferation. CGRP inhibit T cell proliferation. SP enhances immune response and CGRP inhibits immune response. The nervous system and immune system are closely correlated. The nervous system not only perceives the pain sensation/stimuli. Nowadays, we know that nervous system is closely related to our body’s innate and adaptive immune defense mechanism. It’s also important in wound healing. Two important points you have to remember: A-delta fibers (not related to pulpal inflammation but dentin sensitivity) and C-fibers (more related to pulpal inflammation when activated). The nature of the pain is very important. The sharp stabbing pain that last a short period of time dentin sensitivity. If the patient tells you they have dull pain that continues to persist then you have to start to worry about pulpal inflammation. When you get into endodontic, you will learn about reversible and irreversible pulpitis. JUST REMEMBER the differences between A-delta and C fibers.

EXTRA SLIDES IN ORDER